Since upregulation of Fas following reovirus infection is dependent on prodeath signaling via c-Jun N terminal kinase (JNK) [43], and because JNK is activated via a mechanism distinct from NF-κB following reovirus infection [44], we focused our efforts on assessing the regulation and function of death-receptor signaling via TRAIL following reovirus infection. This evidence concerns the gene TNFSF10 and Reoviridae infectious disease.